gout

• Gout


  Genetic factors, diet, comorbidities or certain meds (loop & thiazide diuretics)
• Gout risk factors

  • >30yo, african american, men, beer, food high in purines (shrimp, meat), beverages w high fructose corn syrup, loop/thiazide diuretics, comorbidities (obesity, T2DM, kidney disease)
• Gout history

  Acute, rapid, monoarticular, red, warm, severe joint tenderness/pain, dec ROM, most affected joint is LE big toe, renal nephropathy/nephrolithiasis
• Gout physical exam

  • Tophi (chalky subq nodules made up of MSU crystals in a matrix of protein, mucopolysaccharides and lipids
• Gout lab findings

  Arthrocentesis! Send for culture to make sure it is not an infection, shows pos for MSU needle shaped crystals that are neg for birefringent. CBC (WBC elevated), elevated inflam markers ESR/CRP, elevated serum uric acid
• Gout radiology


  XR "rat bite lesions" (punched out joint erosions), overhanging sclerotic margins
• Gout treatment

  Acute→ corticosteroids, NSAIDs, colchicine, others (do within 24hrs and can be @ home tx). CHRONIC→ stop production w xanthine oxidase inhibitors (allopurinol/febuxostat), promote excretion w uricosuric drugs (probenecid) or uricase (pegloticase)
• Pseudogout


  Arthropathy caused from deposition of Ca pyrophosphate dihydrate (CPPD) crystals in articular tissues
• Pseudogout risk factors

  • Older, W=M, osteoarthritis, previous joint trauma, metabolic/endocrine disease (hyperparathyroidism, hypophosphatasia, hypomagnesemia, Gitelman's syn), familial predisposition
• Pseudogout history

  Rapid, red, swelling, warm, disability, monoarticular (KNEE or wrist/ankle/elbow/toe/shoulder/hip), self-limited but longer than gout flare
• Pseudogout lab findings

  Arthrocentesis showing CPPD crystals with rhomboid shaped crystals and pos birefringent
• Pseudogout radiology

  XR degen changes and chondrocalcinosis AKA cartilage calcification
• Pseudogout treatment

  Treat the inflam as we don't know how to prevent CPPD crystal formation. Corticosteroids, NSAIDs, colchicine. Correct underlying metabolic abnormalities, tx assoc conditions, potential need for further testing
• Pathophysiology of excess uric acid

  Overproduction or underexcretion of uric acid (>6.8mg/dL)
• Pseudogout pathophysiology

  Deposition of DPP crystals in articular tissues (in cartilage near surface of chondrocytes)
• Purine rich diet predisposes for gout/pseudogout
• Thiazide/loop diuretics can cause gout/pseudogout flares
• Pertinent positive/negative history and physical exam findings, and lab/radiology findings can be used to diagnose gout, pseudogout, cellulitis, osteoarthritis and septic joint
• NSAIDs and corticosteroids decrease inflammation in gout and pseudogout. Urate-lowering medications are also needed to prevent continued damage and flares. Colchicine interferes with the inflammatory response.
• First line acute treatment for gout is NSAIDs, corticosteroids and colchicine. First line chronic treatment is allopurinol. First line acute treatment for pseudogout is NSAIDs, corticosteroids and colchicine.
• Gout prevention

  Weight loss, diet modifications (restrict high-fructose corn syrup, limit animal proteins high in purines, avoid ETOH, diet rich in veggies/non-fat/low-fat dairy products) avoid loop and thiazide diuretics
• Pseudogout prevention

  If >3 attacks/yr→proph NSAIDs/colchicine; if chronic CPP crystal inflam arthritis "pseudo-RA" do NSAIDs, colchicine, steroids (hydroxychloroquine +/- methotrexate. Goal is sx management